asthmatics with DEX. Copyright © Qian et al.Vitiligo is a common congenital or acquired disfiguring skin disorder. At present, endoplasmic reticulum (ER) stress has been identified to serve a critical role in the pathogenesis of vitiligo. Receptor-interacting serine/threonine-protein kinase 1 (RIPK1) is a protein serine/threonine kinase. The specific molecular mechanism of RIPK1 in human melanocytes upon ER stress remains to be determined. In the present study, RIPK1 was significantly downregulated in tunicamycin (TM)-induced ER stressed-human melanocytes. Subsequently, to explore the role of RIPK1 in ER stress-induced human melanocytes, human melanocytes were transfected with control or RIPK1 plasmids for 24 h and then treated with 3 ?M TM for 48 h. Reverse transcription-quantitative PCR and western blot analysis indicated that the expression levels of protein kinase R-like endoplasmic reticulum kinase, eukaryotic translation initiation factor 2 subunit 1 and CCAAT-enhancer-binding protein homologous protein were significantly increased in the TM-treated group compared with the controls. In addition, the effect of high RIPK1 expression on ER stress-induced human melanocyte survival was studied. The present results indicated that TM inhibited cell viability and promoted apoptosis in human primary epidermal melanocytes. Western blot analysis demonstrated that the expression of Bax and caspase-3 was upregulated and the expression of Bcl-2 was downregulated in TM-treated human melanocytes. The effects of TM on human melanocytes were reversed by RIPK1 overexpression. Therefore, RIPK1 overexpression may have an effect on the PI3K/AKT/mTOR signaling pathway in human melanocytes under ER stress. The results of the current study demonstrated that RIPK1 could protect human melanocytes from cell damage induced by ER stress by regulating the PI3K/AKT/mTOR and ER stress signaling pathways, thereby serving a protective role in the occurrence and development of vitiligo. Copyright © Sun et al.The usefulness of dressing a surgical wound beyond the first 24-48 h of surgery is currently a controversial issue. The aim of this meta-analysis was to compare the early and delayed removal of dressing following primary closure in the management of clean and contaminated surgical wounds. Systematic searches were conducted in various databases including Medline, Cochrane Controlled Register of Trials (CENTRAL), Scopus, and Embase from January, 1964 until October, 2019. We used the Cochrane risk of bias tool to assess the quality of published trials. We carried out a meta-analysis with random-effects model and reported pooled risk ratios (RR) with 95% confidence intervals (CIs). In total, we analysed 10 studies with 1,708 participants. All the studies were randomized controlled trials, while the majority of studies had unclear or high bias risks. Early dressing removal was favoured with respect to surgical site infection (pooled RR=0.89; 95% CI 0.61 to 1.29), patient's perception on safety (pooled RR=0.60; 95% CI 0.48 to 0.76) and comfort (pooled RR=0.95; 95% CI 0.74 to 1.22), while the remaining outcomes favoured delayed dressing removal. However, none of the factors had statistically significant difference between two interventions except the patient's perception on safety. To summarize, delayed removal of dressing is not superior to early removal following primary closure of clean or clean-contaminated surgical wounds. Copyright © Zhang et al.Current guidelines recommend temporary cessation of clopidogrel for 7-10 days for patients on clopidogrel undergoing colonoscopy with polypectomy. However, recent prospective randomized controlled trials have advocated for uninterrupted clopidogrel, due to similar post-polypectomy bleeding (PPB) rates with and without continued clopidogrel therapy. Thus, a meta-analysis was conducted to assess the risk of PPB rate in patients on continued clopidogrel therapy. Systemically identified publications were used to compare the rate of PPB in patients on continued clopidogrel therapy with those who had interrupted clopidogrel therapy. The primary outcome was the incidence of PPB. The secondary outcomes were immediate PPB, delayed PPB and serious cardio-thrombotic events. This study has been registered in PROSPERO (no. CRD42018118325). https://www.selleckchem.com/products/Dihydroartemisinin(DHA).html A total of five studies were identified, which included 655 patients in the continued clopidogrel group and 6620 patients in the control group. There was an increased risk of PPB with continued clopidogrel [P=0.0003; risk ratio (RR), 1.96; 95% confidence interval (CI), 1.36-2.83). The rate of immediate PPB was slightly higher in the continued clopidogrel group (5.77% vs. 1.77%, respectively), but was not statistically significant (P=0.06; RR, 1.57; 95%CI, 0.98-2.51). The rate of delayed PPB was increased in the continued clopidogrel group (P=0.0008; RR, 3.10; 95%CI, 1.60-5.98). However, no significant difference in serious cardio-thrombotic events was observed within 30 days (P=0.74; RR, 0.78; 95%CI, 0.18-3.40). Although continued clopidogrel therapy decreased the incidence of serious cardio-thrombotic events, the risk of delayed PPB was increased. Therefore, endoscopists should make all preparations to prevent bleeding in the perioperative period for patients at high thrombotic risk and on continued clopidogrel therapy, if polypectomy cannot be reasonably postponed. Copyright © Li et al.MicroRNA (miR)-106b-5p has been reported to act as both an oncogene and tumor suppressor in several tumors. The aim of the present study was to investigate the biological function of miR-106b-5p in osteosarcoma (OS). miR-106b-5p expression was observed to be significantly increased in OS tissues and cell lines. MTT assay and flow cytometry analysis determined that miR-106b-5p inhibitor transfection suppressed OS cell proliferation and induced cell cycle G0/G1 phase arrest. Furthermore, bioinformatics analysis and a luciferase reporter assay demonstrated that cyclin-dependent kinase inhibitor 1A (CDKN1A) was a potential target of miR-106b-5p. p21 protein expression was found to be significantly increased by miR-106b-5p downregulation in OS cells. Further analysis demonstrated that CDKN1A was downregulated in OS tissues and was negatively correlated with miR-106b-5p expression. Furthermore, upregulation of CDKN1A expression mimicked, whilst CDKN1A knockdown reversed the suppressive effects of miR-106b-5p inhibitor on OS cell proliferation and cell cycle progression.